Arrhythmias Flashcards
What are arrhythmias?
Disturbances in heart rate or rhythm that can be caused by changes in impulse formation or impulse conduction
Where do supraventricular arrhythmias arise?
In the atria or AV node
Where do ventricular arrhythmias arise?
In the ventricles
What do alterations in impulse formation involve?
Changes in automaticity, triggered activity
What do abnormalities in impulse conduction arise from?
Re-entry, conduction block, accessory tracts
Rate of pacemaking in the AV node
50-60bpm
Rate of pacemaking in the purkinje fibres
30-40bpm
Overdrive suppression
The SA node pacemaking is the highest and is dominant over other latent pacemakers
What happens if overdrive suppression is lost?
That triggers the latent pacemakers to take over
What can cause loss of overdrive suppression?
SA node firing frequency is pathologically low, conduction of impulse from SA node is impaired, if a latent pacemaker fires at an intrinsic rate faster if SA node despite SA node functioning normally, as a response to tissue damage
Ectopic beat
A heartbeat due to an impulse generated somewhere in the heart outside the AV node. A series of these can generate an ectopic rhythm
What things can cause an ectopic rhythm?
Ischaemia, hypokalaemia, increased sympathetic activity, fibre stretch
Afterdepolarisations
When a normal action potential triggers abnormal oscillations in the membrane potential
Two types of afterdepolarisations
Early afterdepolarisations and delayed afterdepolarisation
When do early afterdepolarisations occur?
During the inciting action potential within late phase 2 (terminal plateau) and early phase 3 (partial repolarisation occurring)
What are early afterdepolarisations occurring in late phase 2 mediated by?
Calcium channels when sodium channels are still closed
What are early afterdepolarisations occurring in early phase 3 mediated by?
Sodium channels
When are early afterdepolarisations most likely to occur?
When heart rate is low
What are early afterdepolarisations associated with?
Purkinje fibres, prolongation of the action potential and drugs that prolong the QT interval
When do delayed afterdepolarisations occur?
After complete repolarisation
What are delayed afterdepolarisations caused by?
Large increases in calcium
How do large increases in calcium result in delayed afterdepolarisations?
Excessive calcium results in oscillatory release of calcium from sarcoplasmic reticulum and a transient inward current that occurs in phase 4
When are delayed afterdepolarisations most likely to occur?
When the heart rate is fast
What can delayed afteredepolarisations be triggered by?
Drugs that increase the calcium influx or release of calcium from the sarcoplasmic reticulum (e.g. digoxin)
Defects in impulse conduction causing arrhythmias
Re-entry, conduction block (through AV node)
What do re-entry arrhythmias involve?
A self sustaining electrical circuit that stimulates an area of the myocardium repeatedly/rapidly
What does the re-entrant circuit require?
Unidirectional block and slowed retrograde conduction velocity
What does unidirectional block involve?
Anterograde conduction is prohibited and retrograde conduction is allowed (action potential goes back through in the ‘wrong’ direction in the damaged cells)
First degree conduction block:
- What happens in this?
- What will be seen on an ECG?
- The tissue conducts all impulses but more slowly than usual
- Long PR interval seen on ECG (>0.2s)
2 types of second degree conduction block
Mobitz type I, Mobitz type II
Describe mobitz type I conduction block
The PR interval gradually increases from cycle to cycle until AV node fails and a ventricular beat is missed
Describe mobitz type II conduction block
The PR interval is constant but every nth ventricular depolarisation is missing
Describe complete conduction block (aka third degree conduction block)
Atria and ventricles beat independently governed by their own pacemakers. Ventricular pacemaker is now the Purkinje fibres – fire relatively slowly and unreliably – manifest as bradycardia and low cardiac output
Example of accessory tract pathway
Bundle of Kent
What is an accessory tract pathway?
An electrical pathway in parallel to the AV node
Describe speed of impulse in Bundle of Kent vs AV node
Impulse through Bundle of Kent is conducted more quickly than the AV node
What happens in the ventricles with an accessory pathway
Ventricles receive impulses from both the normal and accessory pathways – can set up the condition for a re-entrant loop predisposing to tachyarrhythmias
What do anti-arrhythmic drugs generally do?
Inhibit specific ion channels with the intention of suppressing abnormal electrical activity
Vaughn Williams classification of anti-arrhythmic drugs:
- Ia - target and example
- Ib - target and example
- Ic - target and example
- II - target and example
- III - target and example
- IV - target and example
- Ia = Voltage-activated Na+ channel, e.g. Disopyramide
- Ib = Voltage-activated Na+ channel, e.g. Lignocaine
- Ic = Voltage-activated Na+ channel, e.g. Flecainide
- II = beta-adrenoceptor (antagonist), e.g. Metroprolol
- III = Voltage-activated K+ channels, e.g. Amiodarone
- IV = Voltage-activated Ca2+ channels, e.g. Verapamil
Action of class Ia anti-arrhythmic drugs
Associate with and dissociate from Na+ channels at a moderate rate. Slow rate of rise of AP and prolong refractory period
Action of class Ib anti-arrhthymic drugs
Associate with and dissociate from Na+ channels at a rapid rate. Prevent premature beats
Action of class Ic anti-arrhythmic drugs
Associate with and dissociate from Na+ channels at a slow rate. Depress conduction
Action of class II anti-arrhythmic drugs
Decrease rate of depolarization in SA and AV nodes
Action of class III anti-arrhythmic drugs
Prolong AP duration increasing refractory period
Action of class IV anti-arrhythmic drugs
Slow conduction in SA and AV nodes. Decrease force of cardiac contraction
When do class I anti-arrhythmic drugs dissociate from the sodium channel?
In the resting rate
Which anti-arrhythmic drugs would you use to treat arrhythmias in the atria?
Classes IC, III
Which anti-arrhythmic drugs would you use to treat arrhythmias in the ventricles
Classes IA, IB, II
Which anti-arrhythmic drugs would you use to treat arrhythmias in the AV node
Adenosine, digoxin, classes II, IV
Which anti-arrhythmic drugs would you use to treat arrhythmias in the atria and ventricles as well as AV accessory tract pathways
Amiodarone, sotalol, classes IA, IC
What does adenosine do?
Activates A1-adenosine receptors coupled to Gi/o
What does digoxin do?
Stimulates vagal activity
What does verapamil do?
Blocks L-type voltage-activated calcium channels
Supraventricular tachycardia types
Atrial fibrillation, atrial flutter, ectopic atrial tachycardia
Ventricular arrhythmia types
Ventricular ectopics, ventricular tachycardia, ventricular fibrillation, asystole
Clinical causes of arrythmias
Abnormal anatomy, autonomic nervous system, metabolic, inflammatory, drugs, genetic
Causes of tachycardic arrhythmias
Hyperthermia, hypoxia, hypercapnia, cardiac dilation, hypokalaemia
Causes of bradycardic arrhythmias
Hypothermia, hypokalaemia
Symptoms of arrhythmia
Palpitations, SOB, dizziness, loss of consciousness, faintness, sudden cardiac death, angina, heart failure
Investigations for arrhythmia and their effects
ECG, CXR, echocardiogram, stress ECG, 24 hour ECG, event recorder, electrophysiological study
What do sinus arrhythmias involve?
Variations in heart rate, due to reflex changes in vagal tone during the respiratory cycle. Part of ECG is slow and part of the ECG shows faster. This is commonly seen in younger people/younger adults
Sinus bradycardia:
- What is it?
- Causes
- Treatment
- Sinus rhythm with heart rate <60bpm
- Causes can be physiological i.e. athletes, drugs can cause it and it can be caused by ischaemia
- Treatment is atropine or pacing if haemodynamic compromise.
Sinus tachycardia:
- What is it?
- Causes
- Treatment
- Sinus rhythm with heart rate >100bpm
- Physiological (anxiety, fear, hypotension, anaemia), can also be caused by drugs
- Treatment is to treat underlying cause and beta-blockers
Atrial ectopic beats:
- Treatment
No treatment if asymptomatic, beta-blockers may help, avoid stimulants (caffeine, cigarettes)
Regular supraventricular tachycardia:
- What may it be due to?
- Acute management
- Chronic management
- Due to AV nodal re-entrant tachycardia, AV reciprocating tachycardia, ectopic atrial tachycardia
- Acute - Valsava manœuvre, carotid massage, IV adenosine or IV verapamil
- Chronic - avoid stimulants, radiofrequency ablation, beta blockers, anti-arrhythmic drugs
In which patients is radiofrequency ablation first line?
Young, symptomatic patients
Radiofrequency catheter ablation
Selective cautery of cardiac of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re-entry circuit
Radiofrequency catheter ablation procedure
- ECG catheters placed in heart via femoral veins
- Intra-cardiac ECG recorded during sinus rhythm, tachycardia and during pacing manoeuvres to find the location and mechanism of the tachycardia
- Catheter placed over focus/pathway and tip heated to 55-65C
- Cease antiarrhythmic drugs 3-5 days beforehand
Causes of heart block
Ageing process, acute MI, myocarditis, infiltrative disease, drugs, calcific aortic valve disease, port-aorta valve surgery, genetics
Drugs that can cause heart block
Beta-blockers, calcium channel blockers
Which types of heart block indicate pacemaker requirement?
Mobitz type II and complete heart block
Types of pacemakers
Single chamber (only paces right atria or right ventricle), dual chamber (paces both RA and RV)
Ventricular ectopics:
- Causes
- Treatment
- Structural causes (LVH, myocarditis, heart failure), metabolic causes (ischaemic heart disease, electrolytes)
- Treatment is beta blockers or ablation of focus
Ventricular tachycardia causes
Most patients will have significant heart disease (CAD, previous MI), other causes include cardiomyopathy, inherited/familial arrhythmia syndromes
ECG characteristics that help define VTs
- QRS complexes are wide and distorted
- T waves are large with deflections opposite QRS complexes
- Ventricular rhythm is usually regular
- P waves are not usually visible
- PR interval not measurable
Monomorphic VT vs polymorphic VT
Monomorphic VT = QRS complex same all the time
Polymorphic VT = QRS complex changes all the time
Ventricular fibrillation
Chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump
Treatment for ventricular fibrillation
Defibrillation, CPR
Acute treatment for ventricular tachycardia
Direct current cardioversion if unstable, pharmacologic cardioversion with anti-arrhythmic drugs if stable, correct triggers
Long term treatment for ventricular tachycardia
Correct ischaemia if possible, optimise CHF therapies, implantable cardioverter defibrillators if life threatening, VT catheter ablation
What is the most common arrhythmia?
Atrial fibrillation
Forms of atrial fibrillation?
Paroxysmal, persistent, permanent
Paroxysmal atrial fibrillation
Paroxysmal and lasting <48 hours, often recurrent
Persistent atrial fibrillation
Episode lasting >48 hours which can still be cardioverted to sinus rhythm, however unlikely to spontaneously revert to normal sinus rhythm
Permanent atrial fibrillation
Inability of pharmacologic or non-pharmacologic methods to restore to normal sinus rhythm
Associated diseases/causes of atrial fibrillation
Hypertension, congestive heart failure, sick sinus syndrome, coronary heart disease, obesity, thyroid disease, familial, cardiac valve disease, alcohol abuse, congenital heart disease, cardiac surgery, COPD, pneumonia, septicaemia, pericarditis, tumours, vagal cause – high endurance athletes
Symptoms of atrial fibrillation
Palpitations, Pre-syncope, Syncope, Chest pain, Dyspnoea, Sweatiness, Fatigue
ECG changes in atrial fibrillation:
- Atrial rate
- Rhythm
- Recognition
- > 300bpm
- Irregularly irregular
- Absence of P waves and presence of ‘f’ waves
Rate control in the treatment of AF
Digoxin, beta blockers, verapamil, diltiazem
Rhythm control in the treatment of AF:
- Restoration of normal sinus rhythm
- Maintenance of normal sinus rhythm
Restoration - pharmacologic cardioversion - anti-arrhythmic drugs, direct current cardioverson
Maintenance - anti-arrhythmic drugs, catheter ablation surgery
Indications for anticoagulation in AF
Thyrotoxicosis, hypertrophic cardiomyopathy, valvular AF (warfarin only), non-valvular AF with 2 or more risk factors (age >75, hypertension, heart failure, previous stroke, diabetes, CAD
Atrial flutter:
- What is it?
- What is it sustained by?
- How long does it last?
- What may it result in?
- Rapid and regular form of atrial tachycardia, which is usually paroxysmal
- Sustained by a macro-re-entrant circuit confined to the rate atrium
- Episodes last seconds to years
- Can result in thrombo-embolism
Treatment for atrial flutter
Radiofrequency ablation, pharmacologic therapy, cardioversion, warfarin for prevention of thromboembolism
